[Normalization of impairments in deamination of nitrogen compounds in experimental hypercholesterolemia]

Appearance of cadaverine deaminating activity in mitochondrial fractions of liver and kidney of rabbits with experimental alimentary hypercholesterolaemia was prevented by an antioxant diludin (2,6-dimethyl-3,5-diethoxycarbonyl-1,4-dihydropyridine) which also decreased the abnormally elevated AMP-deaminating activity and elevated the decreased monoamine oxidase activity (substrates: serotonin, benzylamine, tyramine). In heart and brain tissues as compared with liver and kidney the impairments caused by hypercholesterolaemia and the normalizing effect of diludin were less distinct. The effects of diludin could be reproduced by nucleophylic reagents sodium thiosulphate or ascorbate. The normalization of impairments in deamination of nitrogenous compounds in hypercholesterolaemia was accompanied by improvement in morpho-physiological manifestations of atherosclerosis (injury of aortal intima, alteration in heart rhythm, changes in content of cholesterol, triglycerides and lipoproteins in blood serum). The data obtained are in agreement with the hypothesis on the significance of qualitative alteration (transformation) in catalytic properties of mitochondrial monoamine oxidases in the mechanism of impairments in deamination of nitrogenous compounds in atherosclerosis.